RESUMO
Obesity is a chronic recurring disease whose prevalence has almost tripled over the past 40 years. In individuals with obesity, there is significant increased risk of morbidity and mortality, along with decreased quality of life. Increased obesity prevalence results, at least partly, from the increased global food supply that provides ubiquitous access to tasty, energy-dense foods. These hedonic foods and the nonfood cues that through association become reward predictive cues activate brain appetitive control circuits that drive hyperphagia and weight gain by enhancing food-seeking, motivation, and reward. Behavioral therapy (diet and lifestyle modifications) is the recommended initial treatment for obesity, yet it often fails to achieve meaningful weight loss. Furthermore, those who lose weight regain it over time through biological regulation. The need to effectively treat the pathophysiology of obesity thus centers on biologically based approaches such as bariatric surgery and more recently developed drug therapies. This review highlights neurobiological aspects relevant to obesity causation and treatment by emphasizing the common aspects of the feeding-inhibitory effects of multiple signals. We focus on glucagon like peptide-1 receptor (GLP-1R) signaling as a promising obesity treatment target by discussing the activation of intestinal- and brain-derived GLP-1 and GLP-1R expressing central nervous system circuits resulting from normal eating, bariatric surgery, and GLP-1R agonist drug therapy. Given the increased availability of energy-dense foods and frequent encounters with cues that drive hyperphagia, this review also describes how bariatric surgery and GLP-1R agonist therapies influence food reward and the motivational drive to overeat.
Assuntos
Peptídeo 1 Semelhante ao Glucagon/uso terapêutico , Hiperfagia/tratamento farmacológico , Obesidade/tratamento farmacológico , Animais , Cirurgia Bariátrica , Terapia Comportamental , Ingestão de Alimentos/fisiologia , Peptídeo 1 Semelhante ao Glucagon/fisiologia , Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas , Humanos , Hiperfagia/complicações , Hiperfagia/metabolismo , Hiperfagia/terapia , Obesidade/etiologia , Obesidade/metabolismo , Obesidade/terapia , Receptores de Glucagon/metabolismo , Redução de Peso/fisiologiaRESUMO
O presente estudo, prospectivo e aberto, foi realizado com objetivo de revisar a eficácia e segurança da fluoxetina em 60 pacientes ambulatoriais do sexo feminino, que apresentavam episódios depressivos maiores, concomitantemente com hiperfagia e obesidade. As pacientes foram submetidas a critérios de inclusäo e exclusäo rígidos e, após serem admitidas no estudo, foram avaliadas nos dias 0, 7, 14, 28, 42 e 56 pela Escala de Hamilton EDH-24 e observadas as perdas ponderais pelo índice de massa corporal de Quetelet. Os resultados demonstraram que a droga é eficaz, melhorando significativamente a depressäo e agindo positivamente na diminuiçäo do peso corporal em consequência do controle de hiperfagia resultante da depressäo
Assuntos
Humanos , Feminino , Depressão/terapia , Fluoxetina/administração & dosagem , Fluoxetina/efeitos adversos , Fluoxetina/uso terapêutico , Obesidade/terapia , Hiperfagia/terapia , Estudos ProspectivosRESUMO
The Eating Disorders Center (EDC), is a clinical-research project of the Mental Research Institute (MRI) centered in the study and treatment of Anorexia Nervosa (Self Starvation), Bulimia (binge-eating and purging) and weight/diet obsessions/compulsions. This paper presents: a) A brief description of the Center, both in its research and clinical aspects. The clinical program is centered in the application of the MRI's brief interactional approach to the treatment of eating disorders. The research project is being developed. b) A definition of terms, taken from the Statistical Manual of Mental Disorders (DSM III) and how these eating disorders have shown an increase in recent years. c) A brief discussion of theories of etiology and maintenance in the field of eating disorders. This point includes the perspective on eating disorders of several theoretical models, and how we believe that it is the societal model the one that can account for the recent increase of eating disorders.